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y3 medicine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

RA definition

A

Chronic, systemic inflammatory disorder characterised by inflammatory polyarthritis

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2
Q

RA aetiology/risk factors

A

Genetics
Family history - 3 fold increase if first-degree relative affected
Demographics - middle-aged females of North American & Western European
Lower socioeconomic status
Smoking
Infections
Occupational exposures

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3
Q

RA pathophysiology

A

Trigger event
Development of self-citrullination (alteration of +ve arginine into neutral citrulline)
Immune system reacts to citrullinated proteins - development of anti-CCP antibodies
Multiple components of the innate and adaptive immune system are activated
Causes infiltration of synovial joints with immune cells and subsequent pro-inflammatory response

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4
Q

RA symptoms

A

Polyarthropathy - MCPJ, wrist joint, PIPJ, knee joint, MTPJ
Joint pain
Joint swelling
Joint stiffness - early morning stiffness lasting > 1 hour
Systemic - myalgia, fatigue, low-grade fever, weight loss and low mood

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5
Q

RA signs

A

Joint swelling
Pain on palpation of joints
Reduced range of movement
Difficulty with fine motor tasks
Muscle atrophy

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6
Q

RA classical signs

A

Boutonniere deformity - flexion at PIPJ with hyperextension of DIPJ
Swan-neck deformity - hyperextension at PIPJ with flexion of DIPJ
Ulnar deviation at MCPs - subluxation of MCPJ with deviation of the fingers towards the ulnar bone
Z-deformity at wrist - hyperextension of IPJ of thumb with carpal bone rotation and radial deviation & ulnar deviation at MCPJ
Hammer toes - compensatory flexion of the toes

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7
Q

RA extra-articular manifestations

A

Ocular - keratoconjunctivitis sicca, episcleritis, scleritis
Oral - xerostoma, oral ulcers
Pulmonary - ILD, serositis, costochondritis
Cardiac - pericarditis, myocarditis, non-infective endocarditis, increased risk of IHD
Renal - glomerulonephritis
Neurological - peripheral neuropathy, entrapment mononeuropathies, cervical myelopathy
Haemotological - neutropenia, thrombocytopaenia/thrombocytosis, haematological malignancies, anaemia of chronic disease
Dermatological - rheumatoid nodules, vasculitis skin rash, pyoderma gangrenosum

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8
Q

RA investigations

A

Bloods - FBC, U&E, bone profile, vit D, LFT, CRP, ESR, autoimmune screen
Rheumatoid factor - IgM autoantibody that reacts against Fc portion of IgG (seen in 60-70% of RA patients)
Anti-CCP - 80% of patients with RA
X-rays - hands and feet
-Soft tissue swelling
-Periarticular osteopaenia
-Joint space narrowing
-Boney erosions
Ultrasound
MRI

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9
Q

RA diagnostic criteria

A

Referred to a rheumatologist for further assessment
ACR/EULAR is a score-based system that looks at 4 domains:
-Joint involvement
-Serology tests (seropositive/seronegative)
-Acute phase reactants (markers of inflammation)
-Patient reported symptoms
Score applied when at least one joint has definitive synovitis & not better explained by another disease
Definite diagnosis = patients scores 6/10 or has erosive boney changes classical of RA

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10
Q

RA general management

A

General care - access to specialist services, holistic monitoring, screening for extra-articular manifestations
Symptom control - NSAIDs, specialist OT, PT

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11
Q

RA pharmacological management

A

Initial therapy - DMARD first line (eg. methotrexate, leflunomide or sulfasalazine)
-In combination with bridging steroid therapy (2-3 months), which allows time for DMARD to take effect
-Methotrexate
-Leflunomide
-Sulfasalazine
-Hydroxychloroquine
Failure to response - combined DMARD ‘step-up’ therapy
Biologic therapy - inadequate response to DMARD & ongoing active disease
-TNF inhibitor - adalimumab, golimumab, infliximab
-Rituximab - anti-CD20 antibody
-Tocilizumab - anti-IL-6 antibody
Managing flares - acute courses of corticosteroids (eg. prednisolone)
Step-down strategy - reducing/stopping therapy in patient who have maintained remission for > 1 year without corticosteroids

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12
Q

RA complications

A

Accelerated atherosclerosis
Associated IHD
Medication side-effects (osteoporosis, higher risk of malignancy)

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13
Q

SLE pathophysiology

A

Exposure of the immune system to blebs from apoptotic cells
The blebs (feature self-antigens) are not efficiently removed and are carried to lymphoid tissue
Immune response is raised when these are taken up by antigen-presenting cells and presented to T-lymphocytes resulting in B-lymphocyte activation & autoantibody production
Failure to inactivate lymphocytes -> circulating autoantibodies & immune-mediated damage to ones own cells

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14
Q

SLE symptoms

A

Fatigue
Malaise
Weight loss
Fever
Myalgia

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15
Q

SLE signs

A

Symmetrical small joint polyarticular arthritis
Malar rash (erythematous rash that lies on the cheeks and across the bridge of the nose)
Photosensitivity & alopecia

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16
Q

SLE extra-articular manifestations

A

Kidneys - nephritis
Lungs - pleurisy, pneumonitis, pleural effusions, pulmonary fibrosis
CVS - pericarditis, myocarditis, heart block
Neuropsychiatric - seizures, ataxia and psychosis
Sjogren’s syndrome
Anaemia of chronic disease

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17
Q

SLE investigations

A

Bedside - vital signs, blood sugar, ECG
Bloods - FBC, U&Es, clotting, LFTs, ESR/CRP, CK, vitamin D3, TFTs
Immunology:
-Antinuclear antibody - positive in about 95% patients with SLE
C3/C4 - low levels seen
-Anti-dsDNA and anti-Smith antibodies - specific for SLE
-Antiphospholipid antibodies - ordered particularly for those who have past history of miscarriages or venous thromboembolism
-Anti-RO/LA and anti-RNP antibodies - poor sensitivity
-Direct coombs test - evidence of haemolytic anaemia
-Immunoglobulins
Urine - urinalysis, random protein:creatinine ratio/24-hr urine collection for protein
Imaging - CXR, MSK XR, renal USS, CT chest, CT/MRI brain, ECHO
Biopsy
Skin - immunofluorescence shows immune deposits at the dermal-epidermal boundary
Kidney - highly sensitive and specific for lupus nephritis

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18
Q

SLE diagnostic criteria

A

EULAR/ACR (2019) - positive ANA is required, then there are ten criteria (clinical and immunological) with patient said to have SLE if they score 10/more points

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19
Q

SLE management

A

Active and healthy lifestyles, regular reviews and optimisation of other medical conditions, use of SPF advised
Induction therapy - aimed at halting disease progression and inducing remission
-Prednisolone and hydroxychloroquine used with combination of others depending on severity (eg. azathioprine, mycophenolate)
Maintenance - preventing relapse, once stable remission is achieved then immunosuppressants can be stopped, with only hydroxychloroquine continuing

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20
Q

SLE complications

A

Thrombosis
Infections
CVS disease
Treatment complications

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21
Q

Ankylosing spondylitis

A

Chronic, multi-system inflammatory disorder characterised by inflammation of the sacroiliac joints & axial skeleton

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22
Q

Ankylosing spondylitis pathophysiology

A

Early sacroiliac joint involvement leading to inflammatory back pain
Followed by involvement of the spine -> initial inflammation at the junction between the vertebrae and intervertebral discs
Annulus fibrosis undergoes ossification & forms syndesmophytes
These may bridge together across multiple vertebrae leading to the classic ‘bamboo’ spine that significantly reduces spinal mobility

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23
Q

Ankylosing spondylitis symptoms

A

Back pain - worse with inactivity, improves with exercise
Neck pain
Alternating buttock pain
Morning stiffness
Fatigue
Arthritis

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24
Q

Ankylosing spondylitis signs

A

Enthesitis - inflammation at the insertion of tendons and ligaments
Positive Schober test - assesses decreases in lumbar spine flexion
Spinal deformity

25
Q

Ankylosing spondylitis extra-articular manifestations

A

Aortitis
Anterior uveitis
AV block
Atlanto-axial instability
Apical lung fibrosis
Amyloidosis
IgA nephropathy

26
Q

Ankylosing spondylitis investigations

A

Bloods - routine, inflammatory markers, HLA-B27 (negative test does not exclude the diagnosis)
X-rays - spinal/pelvic x-rays
Advanced disease:
-Dagger sign - ossification of the supraspinous and interspinous ligaments leading to central radiodense line running up the spine
-Bamboo sign - vertebral body fusion by marginal syndesmophytes & squaring of vertebral bodies, impression of a continuous lateral spinal border
MRI

27
Q

Ankylosing spondylitis diagnostic criteria

A

Patient < 45 years old with a 3 month history of lower back pain should be referred to rheumatologist for assessment of SpA if > 4 of the following criteria are met:
-Onset < 35 years old
-Waking during second half of night
-Buttock pain
-Improves with exercise
-Improves with NSAIDs
-First-degree relative with SpA
-Current/past arthritis
-Current/past enthesitis
-Current/past psoriasis
1984 modified new york criteria
Clinical criteria
-Low back pain >/= 3 months, improved by exercise and not relieved by rest
-Limitation of lumbar spine in sagittal and frontal planes
-Limitation of chest expansion
Radiological criteria
-Bilateral grade 2-4 sacroilitis OR
-Unilateral grade 3-4 sacroilitis
Diagnosis
Definite - radiological criteria present & at least one clinical criterion
Probable - either radiological criterion or 3 clinical criteria present alone

28
Q

Ankylosing spondylitis management

A

Use of non-pharmacological treatments and NSAIDs
Patients with severe disease/non-response to initial therapy - DMARDs, biologics

29
Q

Ankylosing spondylitis complications

A

Spinal fusion
Spinal fractures
Osteoporosis
Restrictive lung disease
Spinal cord injury
Cardiac disease - valvular disease, HF, arrhythmias

30
Q

Gout

A

Crystal arthropathy resulting from excess levels of uric acid leading to precipitation in joints and other tissue

31
Q

Gout aetiology

A

1) Purine overproduction - occurs when there is increased cell turnover/lysis of cells leading to release of purines and breakdown to uric acid
-Myelo- or lymphoproliferative disorders
-Psoriasis
-Use of chemotherapy agents
2) Increased purine intake
-Seafood
-Red meat
-Alcohol
-Fructose-rich beverages
3) Decreased uric acid secretion
-Diuretics
-AKI
-CKD
-ACEi
-Diabetes mellitus

32
Q

Gout pathophysiology

A

Monosodium urate crystals precipitate in peripheral joints - less soluble at low temperatures
Deposition of crystals within joints and soft-tissue may occur asymptomatically (chronic gout) or during acute attacks, crystals trigger an acute inflammatory reaction leading to acutely painful swollen joints

33
Q

Gout symptoms and signs

A

Symptoms
-Joint pain
-Joint swelling
Signs
-Erythema
-Tophi
-Degenerative arthropathy

34
Q

Gout investigations

A

Bloods - serum uric acid
-4-6 weeks following an acute attack
Joint aspiration - gold standard investigation
-Sent for crystal microscopy, microscopy, cultures & sensitives
-Needle-shaped crystals, negatively birefringent of polarised light, monosodium urate crystals
Plain radiographs
-Joint space is maintained
-Lytic lesions in the bone
-Punched out erosions
-Erosions can have sclerotic borders with overhanging edges

35
Q

Gout management

A

Acute management
-General advice - rest, ice & elevation
-First-line therapy - offer NSAIDs or oral colchicine
–Co-prescribe a PPI for gastric protection if giving an NSAID
-Second-line therapy - short course of oral steroids/intra-articular injection of steroids
Prevention
-First-line therapy - allopurinol
–Care must be taken in renal impairment
-Second-line therapy - febuxostat
–Must have LFTs prior & commencing febuxostat

36
Q

Fibromyalgia

A

A syndrome characterised by widespread pain throughout the body with tender points at specific anatomical sites

37
Q

Fibromyalgia symptoms

A

Chronic pain
Lethargy
Cognitive impairment
Sleep disturbance
Headaches
Dizziness

38
Q

Fibromyalgia diagnostic criteria

A

ACR classification criteria
-Lists 9 pairs of tender points on the body
-If patient is tender in at least 11 of these 18 points -> makes diagnosis more likely

39
Q

Fibromyalgia management

A

Difficult and needs to be tailored to the individual patient
Explanation
Aerobic exercise
CBT
Medication - pregabalin, duloxetine & amitriptyline

40
Q

Osteomalacia

A

Describes softening of the bones secondary to low vitamin D levels that in turn lead to decreased bone mineral content

41
Q

Osteomalacia aetiology

A

Vitamin D deficiency
CKD
Coeliac disease
Liver disease
Cirrhosis

42
Q

Osteomalacia pathophysiology

A

Inadequate vitamin D leads to lack of calcium and phosphate in the blood
Low levels result in defective bone mineralisation
Low calcium causes a secondary hyperparathyroidism - parathyroid gland tries to raise calcium level by secreting PTH -> increased reabsorption from bones -> further problems with bone mineralisation

43
Q

Osteomalacia symptoms

A

Fatigue
Bone pain
Muscle weakness
Muscle aches
Pathological/abnormal fractures

44
Q

Osteomalacia investigations

A

Serum 25-hydroxyvitamin D
-<25 nmol/L - vitamin D deficiency
-25 - 50 nmol/L - vitamin D insufficiency
-75 nmol/L or above is optimal
Bloods - calcium, phosphate, ALP, PTH
X-rays
-Osteopenia (more radiolucent bones)
DEXA scan
-Low bone mineral density

45
Q

Osteomalacia management

A

Supplementary vitamin D (cholecalciferol)
-50,000 IU once weekly for 6 weeks
-20,000 IU twice weekly for 7 weeks
-4000 IU daily for 10 weeks
Maintenance supplementary dose of 800 IU should be continued for life after initial treatment
-Patients with vit D insufficiency can be started on this

46
Q

Osteoporosis

A

Characterised by low bone mass and micro-architectural deterioration of bone with resulting fragility and fracture risk
Defined as a bone mineral density of 2.5 SDs below the mean peak mass

47
Q

Osteoporosis pathophysiology

A

Imbalance of bone breakdown & bone formation
-As we age, the activity of osteoclasts increase & not matched by osteoblasts
–Bone mass decreases
-Following menopause, oestrogen deficiency leads to an increased rate of age-related bone loss
–Affects cancellous and cortical bone
-Glucocorticoids - cause increased bone turnover
–Prolonged use can result in a reduced turnover state though even here synthesis is affected more leading to a loss of bone mass

48
Q

Osteoporosis fracture risk

A

Low BMD is associated with a significantly increased risk of fracture
Use of FRAX and QFracture tools are advised to help determine who to investigate further with a DXA
Can be used to calculate the risk of fracture over a 10 year period

49
Q

Osteoporosis investigations

A

Dual-energy X-ray absorptiometry scans are used to assess BMD
-Clinicians may proceed straight to DXA in patients over the age of 50 who have history of fragility fracture/arranged for those younger than 40 with a major risk factor
-Utilises X-rays to assess the density of bones (commonly the hip and spine)
–Normal - T-score > -1
–Osteopenia - T of -1 to -2.5
–Osteoporosis - T score of </= -2.5
Lateral lumbar & thoracic spine radiographs

50
Q

Osteoporosis management

A

Oral bisphosphonates are first-line
-Alendronate - commonly used & is licensed in postmenopausal osteoporosis & osteoporosis in men
–Must be taken in the morning with a glass of water (after fasting overnight)/at least 30 minutes prior to any food or drink
–After taking it the patient must stay upright for 30 mins
-Zoledronic acid - may be used in those not tolerating oral preparations
IV injection once a year
Denosumab - given via s.c. every 6 months
Raloxifene - SORM (may be used in postmenopausal osteoporosis)
HRT

51
Q

Polymyalgia rheumatica

A

Systemic inflammatory disease which is characterised by shoulder and hip girdle pain

52
Q

PR symptoms

A

Bilateral shoulder and/or hip girdle pain
Stiffness and upper limb tenderness - particularly in the mornings
Systemic - low-grade fever, fatigue, weight loss
Low mood
Peripheral - arthritis, swelling and carpal tunnel syndrome

53
Q

PR signs

A

Reduced range of movement
Inability to abduct shoulders past 90 degrees
Synovitis and swelling
Muscles atrophy

54
Q

PR investigations

A

Bloods - FBC, U&E, LFT, ESR/CRP, bone profile, TFT, CK, RF, HbA1c
Specialist bloods - myeloma screen, autoimmune screen
Imaging - CXR, shoulder XR, MSK US, MRI

55
Q

PR diagnostic criteria

A

Should be considered if:
-Age - 50 years or older
-Typical symptoms - bilateral, symmetrical shoulder and/or hip girdle pain associated with stiffness
-Duration - > 2 weeks and lasting > 45 mins at a time
-Elevated ESR/CRP
-Rapid resolution of symptoms with corticosteroids

56
Q

PR management

A

Corticosteroids - oral prednisolone 15mg daily
-Patients should be reviewed in one week to assess the response to treatment
-Should be reduced once symptoms are fully controlled (usually after a period of 3-4 weeks)
-May be over a long period due to risk of relapse/stopping too early
-Need bone protection, gastric protection and BM monitoring
Rheumatology referral - atypical symptoms, problems with steroids
GCA screening and management - high dose corticosteroids

57
Q

PR complications

A

Steroid related (give steroid emergency card)
-Hyperglycaemia
-Mood changes
-Insomnia
-GI bleeding
-Immunosuppression

58
Q

PR follow-up

A

Should be assessed after one week of treatment to assess for a response
Three-monthly within the first year

y3 medicine (10 decks)

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